ABSTRACT Adverse childhood experiences, such as poverty, psychosocial stressors, and environmental hazards, have been consistently linked to poor adult health. Despite the public health significance of such early adversity, the processes by which the ?long arm of childhood? brings about morbidity in later life, including outcomes such as Alzheimer?s disease and related dementias, cardiometabolic disease, and ultimately, mortality, remain largely unknown. Scientific progress in this area has been severely handicapped by two limitations intrinsic to nearly all longitudinal studies of aging: (1) reliance on retrospective assessments of early conditions, and (2) inadequate ?lifespan data? on the intervening processes between childhood and old age. The Boston Early Adversity and Mortality Study (BEAMS) will tackle the limitation of retrospective data by using high-quality administrative record linkage. In Aim 1, we link contemporaneous information on early-life health, family, and environmental hazards from multiple databases (including recently digitalized vital and census records, hospital and military records, public data on water- and air-borne lead exposure) to longitudinal data collected on three cohorts of men who have been assessed repeatedly since 1938 (N=724) or 1961 (N=2280) in the greater Boston area. We extend linkage to siblings of the cohorts to include women and allow within-family comparisons. As the cohorts are 74%-94% deceased, record linkage will create an exceptionally rich, cradle-to-death dataset. In Aim 1, we test the hypothesis that early adversities in the psychosocial (e.g., cold or chaotic family environment), socioeconomic (e.g., impoverished neighborhood), and environmental (e.g., lead exposure) domains have independent and additive effects on poor health in older men and women. To address the second limitation noted above, Aim 2 bridges the knowledge gap on processes which transmit the effects of early adversity onto three age-related outcomes: Alzheimer?s disease and related dementias, cardiometabolic disease, and all-cause mortality. Leveraging the cradle-to-grave data on these cohorts, we test mediational hypotheses regarding deficiency of socioeconomic (low SES) and psychosocial resources (low social support, extraversion, and conscientiousness), and limited cognitive reserve as candidate pathways. We will examine these mediators as age-specific levels and long-term trajectories in adulthood. We will use a coordinated data analytic approach to inform the replicability and generalizability of findings across the 3 socioeconomically-graded cohorts. Completion of these aims will advance state-of-the-art methods and causal knowledge on how multiple dimensions of early conditions affect late life health outcomes such as Alzheimer?s disease and related dementias, cardiometabolic disease, and mortality risk. Findings are expected to inform policy and intervention efforts targeting the upstream determinants of early adversity, and ultimately prolong the span of good health.